Immune Dynamics in Central Nervous System Infections
Summary
The central nervous system (CNS) was once thought to be an immune-privileged site, yet modern research has revealed a rich interplay between resident and infiltrating immune cells that determines the outcome of infections. Microglia, the CNS’s resident myeloid cells, survey the neural milieu and can adopt pro-inflammatory, antiviral, or tissue-repairing phenotypes. Upon neurotropic virus invasion, microglial activation is tightly regulated by intracellular sensors and cross-talk with astrocytes, neurons and peripheral monocyte-derived macrophages. In parallel, CD8+ T lymphocytes patrol the leptomeningeal spaces and parenchyma, contributing to viral clearance but also posing a risk of immunopathology if their responses become excessive. Cytokines such as type I interferons mediate antiviral states in multiple cell types, while alarmins and chemokines recruit monocytes across the blood–brain barrier. Single-cell analyses now reveal dynamic transcriptional programmes in microglia and infiltrating monocytes, showing how they shift from homeostatic to antiviral and then to immune-cell recruiting states during acute encephalitis. The balance between pathogen control and limiting immune-mediated damage underpins both survival and neurological sequelae. Understanding these immune dynamics is crucial for the development of targeted interventions that bolster antiviral defence without provoking harmful inflammation.
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Immune Dynamics in Central Nervous System Infections publication trend
The graph below shows the total number of articles in immune dynamics in central nervous system infections across all publications each year (not limited to Nature Index journals).
Technical terms
Microglia: Resident macrophage-like cells of the CNS that monitor tissue integrity and initiate immune responses.
Monocyte-derived macrophages: Peripheral monocytes recruited into the CNS that differentiate into macrophages and contribute to inflammation and repair.
MAVS: Mitochondrial antiviral-signalling protein that triggers downstream interferon production in response to viral RNA detection.
Interferon: Family of cytokines that establish an antiviral state by upregulating interferon-stimulated genes in infected and neighbouring cells.
IL-33: An alarmin cytokine released by CNS cells that binds ST2 on microglia to promote their activation and survival.
ST2: Receptor for IL-33 expressed on microglia and other immune cells, mediating tissue-protective signalling.
References
- MAVS signaling shapes microglia responses to neurotropic virus infection. Journal of Neuroinflammation (2024).
- Temporal tracking of microglial and monocyte single-cell transcriptomics in lethal flavivirus infection. Acta Neuropathologica Communications (2023).
- Oligodendrocyte-derived IL-33 functions as a microglial survival factor during neuroinvasive flavivirus infection. PLOS Pathogens (2023).
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